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Since this article has been suspected of research misconduct and the corresponding authors did not respond to our request to prove originality of data and figures, "Long noncoding RNA SNHG7 represses the expression of RBM5 to strengthen metastasis of hepatocellular carcinoma, by B.-Z. Sun, D.-G. Ji, Z.-X. Feng, Y. Wang, published in Eur Rev Med Pharmacol Sci 2019; 23 (13): 5699-5704-DOI: 10.26355/eurrev_201907_18307-PMID: 31298322" has been withdrawn. The Publisher apologizes for any inconvenience this may cause. https://www.europeanreview.org/article/18307.
RESUMEN
OBJECTIVE: Long noncoding RNAs (lncRNAs) have been reported to be vital in tumor progression. Hepatocellular carcinoma (HCC) is a common type of fatal primary liver cancers worldwide. This study aims to determine whether lncRNA SNHG7 (small nucleolar RNA host gene 7) functions in the metastasis of HCC. PATIENTS AND METHODS: Quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) was conducted to detect the SNHG7 expression in HCC cells and tissue samples. Moreover, function assays were performed in vitro to identify the role of SNHG7 in metastasis of HCC cells. Western blot assay was used to explore the possible mechanism. RESULTS: SNHG7 expression was remarkably higher in HCC tissues than that in adjacent tissues. Moreover, HCC migration and invasion were suppressed after silence of SNHG7 in HCC cells. Moreover, after silence of SNHG7, RBM5 was upregulated in HCC cells. Besides, the expression of RBM5 in tumor tissues was negatively correlated to the expression of SNHG7. CONCLUSIONS: Our study suggests that SNHG7 could promote cell invasion and migration in HCC cells through downregulating RBM5, which may offer a new therapeutic intervention for HCC patients.
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Carcinoma Hepatocelular/metabolismo , Proteínas de Ciclo Celular/antagonistas & inhibidores , Proteínas de Unión al ADN/antagonistas & inhibidores , Neoplasias Hepáticas/metabolismo , ARN Largo no Codificante/metabolismo , Proteínas de Unión al ARN/antagonistas & inhibidores , Proteínas Supresoras de Tumor/antagonistas & inhibidores , Carcinoma Hepatocelular/patología , Proteínas de Ciclo Celular/genética , Proteínas de Ciclo Celular/metabolismo , Movimiento Celular , Proteínas de Unión al ADN/genética , Proteínas de Unión al ADN/metabolismo , Células Hep G2 , Humanos , Neoplasias Hepáticas/patología , ARN Largo no Codificante/genética , Proteínas de Unión al ARN/genética , Proteínas de Unión al ARN/metabolismo , Células Tumorales Cultivadas , Proteínas Supresoras de Tumor/genética , Proteínas Supresoras de Tumor/metabolismoRESUMEN
OBJECTIVE: To elucidate the biological functions of long non-coding RNA (lncRNA) SNHG7 in breast cancer (BC), and its underlying mechanism in the occurrence and progression of BC. PATIENTS AND METHODS: The expression of SNHG7 in 72 pairs of BC tissues and paracancerous tissues was detected by quantitative Real-time polymerase chain reaction (qRT-PCR). Correlation between SNHG7 expressions with pathological indicators of BC patients was analyzed. Similarly, SNHG7 expression in BC cell lines was determined by qRT-PCR as well. After constructing the small inference RNA of SNHG7, cell proliferation, migration and invasion were determined by cell counting kit-8 (CCK-8), 5-Ethynyl-2'-deoxyuridine (EdU) and transwell assay. MicroRNA-186 expression in BC tissues and cells was accessed. Dual-luciferase reporter gene assay was conducted to verify the binding condition between SNHG7 and microRNA-186. RESULTS: SNHG7 expression was higher in BC tissues than that of paracancerous tissues. High expression of SNHG7 was positively correlated to tumor stage, lymph node metastasis and distant metastasis, whereas not correlated to age, sex and tumor location of BC. Kaplan-Meier curves revealed that higher expression of SNHG7 is correlated to the worse prognosis of BC patients. SNHG7 was highly expressed in BC cells as well. Knockdown of SNHG7 inhibited proliferative, invasive and migratory abilities of BC cells. QRT-PCR data showed that microRNA-186 is lowly expressed in BC tissues compared with that of paracancerous tissues. MicroRNA-186 was lowly expressed in BC cells as well. Both mRNA and protein levels of microRNA-186 were negatively correlated to SNHG7 in BC tissues. Finally, the dual-luciferase reporter gene assay demonstrated that SNHG7 could be directly targeted by microRNA-186. CONCLUSIONS: SNHG7 is highly expressed in BC, which is correlated to tumor stage, lymph node metastasis and distant metastasis of BC patients. SNHG7 could promote malignant progression of BC by regulating microRNA-186.
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Neoplasias de la Mama/genética , MicroARNs/genética , ARN Largo no Codificante/genética , Neoplasias de la Mama/patología , Línea Celular Tumoral , Movimiento Celular/genética , Proliferación Celular/genética , Femenino , Regulación Neoplásica de la Expresión Génica , Humanos , Metástasis Linfática , Células MCF-7 , Masculino , Persona de Mediana EdadRESUMEN
OBJECTIVE: Hepatocarcinoma is a great threat to global health. MicroRNA-23a was suggested to regulate growth and apoptosis in certain cell lines. Our study was focused on growth, proliferation, and apoptosis of hepatocarcinoma cell line MHCC97H under the influence of microRNA-23a, and explored the mechanism of pro-apoptosis microRNA-23a. MATERIALS AND METHODS: MicroRNA-23a and control microRNA (scramble miRNA, for short as miRNA) were synthesized with the routine protocol. Lipofection transfection was performed in hepatocarcinoma cell line MHCC97H. 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) assay, caspase-3 activity detection, and flow cytometry were performed to examine growth, proliferation, and apoptosis of hepatocarcinoma cell line MHCC97H, respectively. Kidney inhibitor of apoptosis protein (KIAP) and small interfere RNA (siRNA) was synthesized for inhibition of KIAP. KIAP plasmid was established for activation of KIAP. Western blot was performed to examine the protein expression of KIAP and caspase protein family after transfection of KIAP siRNA or KIAP plasmid. RESULTS: Compared with miRNA transfection, microRNA-23a transfection significantly reduced the growth of MHCC97H cells, and decreased the expression of KIAP (p < 0.05). Enhanced translocation of phosphatidylserine and activation of caspase-3 were observed in microRNA-23a transfection cells. Moreover, inhibition of KIAP enhanced the pro-apoptosis effect of microRNA-23a, while activation of KIAP abrogated pro-apoptosis effect of microRNA-23a. CONCLUSIONS: MicroRNA-23a inhibits growth and proliferation of MHCC97H cells, and induces apoptosis of MHCC97H cells via down-regulating KIAP. KIAP could be a potential therapeutic target for hepatocarcinoma treatment.